Linked Life Data

15737621

Source:http://linkedlifedata.com/resource/pubmed/id/15737621

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2005-3-1
pubmed:abstractText
Expression of alpha-cardiac myosin heavy chain gene (alphaMHC) is developmentally regulated in normal embryonic hearts and down-regulated in cardiac myopathy and failing hearts. Jumonji (JMJ) has been shown to be critical for normal cardiovascular development and functions as a transcriptional repressor. Here, we demonstrate that JMJ represses alphaMHC expression through inhibition of myocyte enhancer factor 2 (MEF2) activity. In primary cardiomyocytes, overexpression of JMJ leads to marked reduction of endogenous alphaMHC expression. JMJ represses the synergistic activation of alphaMHC by MEF2 and thyroid hormone receptor (TR). Interestingly, JMJ inhibits transcriptional activities of all MEF2 isoforms, but not the TR-dependent activation. The transcriptional repression domain of JMJ interacts with the N-terminal part of MEF2A, resulting in the repression of MEF2A activities. These results suggest that JMJ represses alphaMHC expression via protein-protein interaction with MEF2A.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0006-291X
pubmed:author
pubmed:issnType
Print
pubmed:day
8
pubmed:volume
329
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
544-53
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
Jumonji represses alpha-cardiac myosin heavy chain expression via inhibiting MEF2 activity.
pubmed:affiliation
Department of Anatomy and Cardiovascular Research Center, University of Wisconsin Medical School, Madison, WI 53706, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't